AI Article Synopsis
- Chronic intermittent hypoxia (CIH) leads to increased arterial pressure and reduced vasodilatory response to acetylcholine, while treatment with losartan (Los) mitigates these effects.
- After 28 days, the study shows that CIH raised blood pressure and lowered vasodilation compared to normal conditions (NORM), and this vascular dysfunction was countered by Los treatment.
- Changes in angiotensin II receptor expression were noted in the CIH group, suggesting that the vascular issues caused by CIH are related to the renin-angiotensin system (RAS) signaling.
Article Abstract
Chronic intermittent hypoxia (CIH) raises arterial pressure, impairs vasodilator responsiveness, and increases circulating angiotensin II (Ang II); however, the role of Ang II in CIH-induced vascular dysfunction is unknown. Rats were exposed to CIH or room air (NORM), and a subset of these animals was treated with losartan (Los) during the exposure period. After 28 days, vasodilatory responses to acetylcholine or nitroprusside were measured in isolated gracilis arteries. Superoxide levels and Ang II receptor protein expression were measured in saphenous arteries. After 28 days, arterial pressure was increased and acetylcholine-induced vasodilation was blunted in CIH vs. NORM, and this was prevented by Los. Responses to nitroprusside and superoxide levels did not differ between CIH and NORM. Expression of AT(2)R was decreased and the AT(1)R:AT(2)R ratio was increased in CIH vs. NORM, but this was unaffected by Los. These results indicate that the blood pressure elevation and endothelial dysfunction associated with CIH is dependent, at least in part, on RAS signaling.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3409315 | PMC |
| http://dx.doi.org/10.1016/j.resp.2012.05.025 | DOI Listing |
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